Studies suggest that the production of endogenous antiinflammatory agents during sepsis reduces host defense and predisposes to subsequent infection. Whether such a state of immunosuppression during sepsis actually exists or is reversible with the administration of proinflammatory agents is unclear. However, use of recombinant granulocyte colony stimulating factor (G-CSF) to augment host defense following the onset of sepsis in critically ill patients has been proposed. Using a rat model, we plan to determine whether an initial episode of infection and sepsis augments the host defense effects of G-CSF during a subsequent episode.